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Updated: Aug 15, 2026
A Primary Neuron Culture System for the Study of Herpes Simplex Virus Latency and Reactivation
Published on: April 2, 2012
The isolation and characterization of mutants of herpes simplex virus type 1 that induce cell fusion
Abstract:
Six cell fusion-causing syn mutants were isolated from the KOS (syn-101 to syn-106) and three from the HFEM (syn-109) strains of herpes simplex virus type 1 (HSV-1). The mutants were studied by complementation and recombination with syn-20 (a syncytial mutant of KOS) and ts-B5 (a syncytial mutant of HFEM). Some studies also employed MP, a syncytium-inducing strain isolated from the non-syncytial parent, mP. Complementation and recombination of syn-20 and ts-B5 indicated that these two mutants were altered in two different virus genes. The recombination frequency between syn-20 and ts-B5 was very similar to that observed between MP and ts-B5, indicating the syn-20 and MP may represent alterations in the same virus gene. syn-101, syn-103, syn-104 and syn-105 were tentatively assigned to the syn-20 complementation group, while syn-107 and syn-109 were tentatively assigned to the ts-B5 complementation group, syn-106 and syn-108 were excluded from the ts-B5 group. syn-102 could not be excluded from either complementation group. syn-101 induced markedly less fusion at 38 degrees C relative to 34 degrees C. At 34 degrees C the patterns of syn-101-infected cell peptides and glycopeptides, examined by SDS-gel electrophoresis, were normal, but at 38 degrees C the amount of glycopeptide gC was particularly reduced. syn-102 produced decreased amounts of glycoproteins, and a non-glycosylated peptide, probably ICP6, was absent from extracts infected with syn-106.
Insights
Herpes simplex virus type 1 (HSV-1) syncytial mutants were analyzed using complementation and recombination. This research identified alterations in specific HSV-1 genes responsible for cell fusion and glycoprotein production.
Area of Science:
- Virology
- Molecular Biology
- Genetics
Background:
- Herpes simplex virus type 1 (HSV-1) can cause cell fusion, a process mediated by specific viral genes.
- Understanding the genetic basis of HSV-1-induced syncytia formation is crucial for comprehending viral pathogenesis.
- Previous studies have identified syncytial (syn) mutants, but their precise genetic alterations require further characterization.
Purpose of the Study:
- To genetically map and characterize newly isolated HSV-1 syncytial mutants.
- To identify the specific viral genes responsible for cell fusion and syncytia formation.
- To investigate the impact of these mutations on viral protein and glycoprotein synthesis.
Main Methods:
- Isolation of six cell fusion-causing HSV-1 mutants (syn-101 to syn-106) from KOS and one (syn-109) from HFEM strains.
- Complementation and recombination analyses were performed using established syncytial mutants syn-20 and ts-B5, and strain MP.
- Analysis of viral peptides and glycopeptides in infected cells using SDS-gel electrophoresis at different temperatures.
Main Results:
- Complementation and recombination studies indicated that syn-20 and ts-B5 affect two distinct HSV-1 genes.
- Mutants syn-101, syn-103, syn-104, and syn-105 were assigned to the syn-20 complementation group; syn-107 and syn-109 to the ts-B5 group.
- Mutant syn-101 showed temperature-sensitive fusion and reduced glycoprotein gC at the non-permissive temperature; syn-102 exhibited decreased glycoproteins, and syn-106 lacked ICP6.
Conclusions:
- The study successfully assigned several HSV-1 syncytial mutants to specific complementation groups, implicating distinct viral genes in cell fusion.
- Mutations in specific HSV-1 genes directly impact viral glycoprotein synthesis, including gC and potentially ICP6, affecting cell-cell fusion.
- These findings contribute to a deeper understanding of the molecular mechanisms underlying HSV-1-mediated cell fusion and pathogenesis.
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